Cholelithiasis in patients treated with a very-low-calorie diet.

One hundred seventy-nine obese patients (mean body mass index = 36.3) were retrospectively evaluated for the development of cholelithiasis associated with the use of a 2530-kJ/d (605-kcal) very-low-calorie diet (VLCD). Nine percent of patients had preexisting gallstones and 11% of patients developed gallstones either during or within 6 mo of completing the diet. Six percent had subsequent cholecystectomy. Ursodeoxycholic acid administered to one patient resulted in spontaneous stone dissolution whereas spontaneous dissolution occurred in three patients. Surveys of patients at three other programs using the same diet yielded similar incidence of gallstones. We conclude that rapid weight loss associated with the use of VLCD is associated with a significant incidence of gallstone formation. VLCD should be physician supervised because resolution of cholelithiasis spontaneously, with stone passage, or dissolution with ursodeoxycholic acid therapy may reduce the need for cholecystectomy.

Body composition and weight maintenance with a very-low-calorie diet for the treatment of moderate obesity.

We report body composition in 11 moderately obese patients (mean BMI less than 30) treated for 8 wk with a 2530-kJ/d (605-Kcal) diet. Mean weight loss was 9.4 kg. Fat-free mass (FFM) loss of 2.3 kg was 23% of total weight loss and essentially equal to loss of total body water (2.5 L). Body composition was measured by the Futrex-5000 near-infrared technique. We conclude there is no excess loss of FFM in moderately obese patients treated with MNP 70/70, a 70-g protein, 70-g carbohydrate dietary supplement for 8 wk.

Repeated use of the very-low-calorie diet in a structured multidisciplinary weight-management program.

Forty-eight obese patients (mean body mass index = 36.4) were retreated with a very-low-calorie diet (VLCD) at a mean of 104-wk after first VLCD. Mean weight regain was 23 kg or 86% regain of initial loss. Retreatment with VLCD required weekly physician monitoring and indepth psychotherapy group attendance. Five patients (10%) lost an average of 4.55 kg and withdrew within the first 4 wk (group AO. Thirteen patients (27%) lost 13.8 kg over 11.5 wk, an average weight loss of 1.2 kg/wk and enrolled in maintenance (group B). Thirty patients (63%) lost 10.2 kg over 20 wk, an average weight loss of 0.5 kg/wk and did not enroll in the maintenance program (group C). Although weight loss occurs in patients retreated with the VLCD, adherence to the VLCD and commitment to the maintenance program are not optimal.

Calcium homeostasis in patients with acute pancreatitis.

Calcium homeostasis was studied serially in six patients admitted to the surgical intensive care unit because of acute pancreatitis. All developed ionized hypocalcemia. Serial assays of serum parathyroid hormone (PTH) revealed a prompt response to this hypocalcemia (1143 +/- 239 versus 574 +/- 24 pg/ml, P less than 0.05). Serum 1,25-dihydroxyvitamin D (1,25(OH)2D) levels rose from 26 +/- 8 to 104 +/- 17 pg/ml (P less than 0.01) in the expected time frame subsequent to the PTH peak, confirming the biologic significance of the PTH increases observed. Despite these significant elevations of PTH and 1,25(OH)2D, the expected prompt return of ionized calcium concentrations to normal levels was not seen. Also, urinary cyclic adenosine monophosphate production was not stimulated. These results suggest an acute functional resistance of bone to physiologic levels of PTH stimulation during the acute phase of pancreatitis. Fluid sequestration and hypovolemia are marked at this time. We suggest that pancreatitic hypocalcemia may occur when oligemic bone cannot respond normally to PTH and 1,25(OH)2D stimulation. As such, it may represent an end organ failure syndrome associated with shock and poor tissue perfusion.